The field of the invention is systems and methods for cardiac rhythm and heart failure management. More particularly, the invention relates to systems and methods for performing cardiac resynchronization therapy in which adjustments to pacing control parameters are automatically made in relation to a model of cardiac electrical activity, such as a model of global cardiac electrical activity.
Electrical therapies are targeted toward patients who have heart failure associated with cardiac timing abnormalities. This is due to optimal cardiac pump function depending on a condition of methodical arrangement of component parts that is precisely and dynamically orchestrated by electrical timing. This electromechanical ordering occurs at multiple anatomic levels, including within atria, between atria and ventricles, between ventricles, and especially within the left ventricle. Improper electrical timing disrupts these systematic arrangements, can occur in isolation or in various combinations at any anatomic level, and degrades cardiac pump function.
Conduction delay within the left ventricle, caused by left bundle branch block (“LBBB”) and often accompanied by an atrioventricular delay, defines asynchronous heart failure. More specifically, left ventricular conduction delay due to bundle branch block causes regional heterogeneity in contraction and stretch, or asynchrony, which reduces pump function and stimulates negative left ventricular remodeling, characterized by increased chamber volumes. Experimental models have demonstrated a direct linkage between left ventricular electrical activation, cardiac mechanics, and remodeling. The conceptual basis of multisite pacing, which is also referred to as cardiac resynchronization therapy (“CRT”) or biventricular pacing, for asynchronous heart failure is to minimize ventricular conduction delay, which reduces contractile asynchrony and improves chamber mechanics.
Minimization of left ventricle electrical activation asynchrony (termed “resynchronization”) restores part or all of the LBBB-induced impairment in left ventricle mechanics. Resynchronization induces so-called “reverse” remodeling, characterized by ventricular volume reductions, and improved pump function, characterized by increased ventricular ejection fraction. As a result, reverse remodeling is also associated with reduced heart failure morbidity and mortality. In addition, proper adjustment of atrioventricular timing, a second order effect of CRT, maximizes left ventricle preload and diastolic filling. Accordingly, CRT can improve pump function by both unloading the asynchronous left ventricle during contraction and maximizing left ventricle preload during filling, though these two effects are independent of each other since optimal atrioventricular timing for diastolic function is not required for ventricular electromechanical resynchronization and plays no role in reverse volumetric ventricular remodeling, and reverse remodeling can occur even when the atrioventricular relationship is improperly timed or nonexistent.
The translational mechanism for resynchronization and reverse volumetric remodeling in response to multisite pacing for asynchronous heart failure is ventricular activation wavefront fusion, which is evident on a paced 12-lead surface ECG. Presence of ventricular activation wavefront fusion predicts increased probability of reverse remodeling, whereas absence of wavefront fusion predicts reduced probability of remodeling, regardless of baseline substrate conditions.
Unfavorable substrate conditions, such as high myocardial scar volume or small amounts of ventricular conduction delay, cannot be modified by pacing techniques. In contrast, pacing strategies can be readily adapted to modify ventricular activation, for example, to induce ventricular activation wavefront fusion, and such instructions can be implemented automatically in the fully ambulatory patient having a cardiac implantable electrical device (“CIED”). However, recent experimental evidence indicates that only two-thirds of CIED patients have paced surface ECG evidence of ventricular activation wavefront fusion during conventional CRT. This implies that a large inter-patient heterogeneity exists among clinical responders, and that failure to correct ventricular conduction delay, despite conventional CRT pacing, contributes significantly to volumetric remodeling non-response.
It would therefore be desirable to provide a system and method for cardiac resynchronization therapy that utilizes measurements correlated with improvement in clinical outcome measures, such as heart failure morbidity and mortality and, most notably, reverse volumetric remodeling. It would be further desirable to have a system and method that more accurately characterize CRT response patterns on a patient-specific basis and that result in clinically reliable measurements and changes to pacing control parameters.